Researchers are looking for XMRV in CFS in the immune cells (T and B and others) in the blood. The papers indicated that the genetic sequences of the virus in T and B cells can get altered (or edited) over time by what are called APOBEC3 editing enzymes. Cells use these enzymes to attack retroviruses that have become integrated into our genome. Simply by exchanging the guanine bases in the retroviral sequences to adenine APOBEC3 stops the virus from replicating. Basically, except for the few virions that manage to escape this defense mechanism, T and B cells in the blood are a dead end for XMRV.

The XMRV in prostate cancer cells may be different, however, because the APOBEC3 enzyme is not found in those cells, thus allowing them to escape this editing process. Since XMRV was first discovered in prostate cancer cells it's not surprising that prostate cancer XMRV forms the basis for many of the PCR probes but it does mean studies using this form of the XMRV could miss the different looking virus in the T and B cells

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Is there growing concensus for the two versions of XMRV theory. There may have been an oblique reference to this in Amy Dockser Marcus' latest article:

...there is a growing sense that virus taken from patients may be different than the virus the labs studied.

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Have the prostate cancer and the negative studies researchers been working on just the prostate version while WPI has only been working on the ME/CFS version? Could it really be as simple as that? All the debate about cohorts, methodologies etc will go up in smoke. New questions would then need to be raised. How did this happen? Who is to blame?